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ABSTRACT: RNA-seq for MTB infected mice BMDMs

PROVIDER: PRJNA723409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14290429.fastq.gz	Fastqsanger.gz
	SRR14290430.fastq.gz	Fastqsanger.gz
	SRR14290431.fastq.gz	Fastqsanger.gz
	SRR14290432.fastq.gz	Fastqsanger.gz
	SRR14290433.fastq.gz	Fastqsanger.gz

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Effects of type I IFN signaling on gene expression of Mycobacterium tuberculosis-infected bone marrow-derived macrophages (BMDMs)

Project description:Our previous work identified that type I IFNs mediate macrophage death after infection of Mycobacterium tuberculosis (Mtb) through a novel mechanism.Type I IFN signaling relies on its several hundred ISGs to execute various functions. In order to delineate the downstream mechanism of type I IFN-mediating cell death, we adopted RNA-seq experiments to identify which gene(s) are differentially expressed in WT or Ifnar1-/- bone marrow-derived macrophages (BMDMs). In the meantime, we're also interested in how genetic background affects transcriptomics in BMDMs infected with Mtb. Thus a transcriptomics analysis of C57BL/6, 129S2 and 129X1 infected with Mtb were also conducted.

2025-02-13 | GSE289356 | GEO

Effect of small molecule inhibitors on transcriptome of B6.Sst1S bone marrow derived macrophages stimulated with TNF and infected with virulent Mycobacterium tuberculosis

Project description:We investigated candidate host-directed therapies for tuberculosis in vitro. BMDMs from tuberculosis susceptible mice B6.Sst1S were stimulated with TNF and infected with Mtb. The infected macrophage were treated with Rocaglamide A, ISRIB and JNK inhibitor SP600125 alone or in combinations to asses the inhibitors' effectas on macrophage transcriptome.

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Tax1bp1 enhances bacterial virulence and promotes inflammatory responses during Mycobacterium tuberculosis infection of alveolar macrophages

Project description:Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. Mycobacterium tuberculosis (Mtb) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during Mtb infection and the variation of the response in different macrophage subtypes remain obscure. Here, we show that the autophagy receptor Tax1bp1 plays a critical role in enhancing inflammatory cytokine production and increasing the susceptibility of mice to Mtb infection. Surprisingly, although Tax1bp1 restricts Mtb growth during infection of bone marrow-derived macrophages (BMDMs) (Budzik et al. 2020) and terminates cytokine production in response to cytokine stimulation or viral infection, Tax1bp1 instead promotes Mtb growth in AMs, neutrophils, and a subset of recruited monocyte-derived cells from the bone marrow. Tax1bp1 also leads to increases in bacterial growth and inflammatory responses during infection of mice with Listeria monocytogenes, an intracellular pathogen that is not effectively targeted to canonical autophagy. In Mtb-infected AMs but not BMDMs, Tax1bp1 enhances necrotic-like cell death early after infection, reprogramming the mode of host cell death to favor Mtb replication in AMs. Tax1bp1’s impact on host cell death is a mechanism that explains Tax1bp1’s cell type-specific role in the control of Mtb growth. Similar to Tax1bp1-deficiency in AMs, the expression of phosphosite-deficient Tax1bp1 restricts Mtb growth. Together, these results show that Tax1bp1 plays a crucial role in linking the regulation of autophagy, cell death, and pro-inflammatory host responses and enhancing susceptibility to bacterial infection.

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Effect of hypoxia on Mycobacterium tuberculosis-host phagocyte interactions

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Project description:The BCG vaccine has been used against tuberculosis (TB) for over hundred years; however, it does not protect adults from pulmonary TB. To develop alternative vaccines against TB, we generated Mycobacterium tuberculosis H37Rv (Mtb)-derived vaccine strains by rationally deleting key virulent genes, resulting in single (SKO; ΔfbpA), double (DKO; ΔfbpA-ΔsapM), triple (TKO-D; ΔfbpA-ΔsapM-ΔdosR and TKO-Z; ΔfbpA-ΔsapM-Δzmp1), and quadruple (QKO; ΔfbpA-ΔsapM-Δzmp1-dosR) strains. To understand how macrophages, the host cells that defend against infection and process antigens for presentation to immune cells, respond to these vaccine strains, we performed transcriptomic analyses of mouse bone marrow-derived macrophages (BMDMs) infected with these strains. The transcriptomic data were compared with similar data obtained from macrophages infected with Mtb H37Rv and BCG. Our analyses revealed that genes associated with various immune and cell signaling pathways, such as NF-kappa B signaling, TNF signaling, cytokine-cytokine receptor interaction, chemokine signaling, hematopoietic cell lineage, Toll-like receptor signaling, IL-17 signaling, Th1 and Th2 cell differentiation, Th17 cell differentiation, and T cell receptor signaling were differentially expressed in BMDMs infected with our vaccine strains. Enhanced expression of cytokines and chemokines, including proinflammatory cytokines such as TNF-α, IL-6, GM-CSF, and IL-1, which are essential for the immune response against Mtb infection, was also observed in BMDMs infected with these strains. In particular, BMDMs infected with all vaccine strains exhibited a significant upregulation of genes associated with the IL-17 pathway. These results may indicate that our vaccine strains could induce a protective immune response against TB.

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| PRJNA1150773 | ENA